1. Hela cells contain Beta-adrenergic receptors (BetaAR) but respond poorly to Beta-agonists. Cells treated with butyrate (Bu) become highly responsive and acquire more BetaAR. By using membrane fusion techniques, BetaAR from control and Bu-treated cells were shown to be equally effective in stimulating adenylate cyclase (AC) in membranes that lack BetaAR. Bu also induced an increase in GTP-binding components (N) as measured by cholera toxin-catalyzed ADP-ribosylation and reconstitution into cyc- membranes that lack N. Both N from control and Bu-treated HeLa were able to couple AR and AC present in cyc- membranes. Thus, Bu induces not only AC components in HeLa but also increased coupling of the components. 2. Incubation of membranes from human fibroblasts with either Beta-agonists or PGE1 results in desensitization of AC. The process is time and temperature dependent and requires GTP. As was observed in intact cells, PGE1 causes a heterologous desensitization whereas Beta-agonists cause a homologous one. 3. When exposed to hCG, murine Leydig tumor cells lose their responsiveness to hCG (desensitization), their hCG receptors (downregulation) and degrade bound hCG in that temporal sequence. Preliminary results indicate that initially the receptors become uncoupled from AC, then internalized and degraded along with bound hCG.